DNMT1 and neoplasm: Based on this work, Stone et al. [243] further demonstrated that the activation of type I interferon signaling in response to DNMT inhibitor 5-azacytidine was a key requirement for efficient stimulation of CD45+ (leukocyte common antigen) immune cells, CD8+ cytotoxic T cells, natural killer cells, restriction of macrophages, and myeloid-derived suppressor cells in the ovarian TME in vivo, prompting the inhibition of tumor growth and increased survival.